Resuscitation treatments for patients suffering from cardiac arrest generally include clearing and opening the patient's airway, providing rescue breathing or ventilation with a manually operated bag-valve or powered portable ventilator apparatus for the patient, and applying chest compressions to provide blood flow to the victim's heart, brain and other vital organs. The chest compressions may be delivered by manually compressing the patient's chest in the region of the sternum or by the use of a powered chest compressor. If the patient has a shockable heart rhythm, resuscitation also may include defibrillation therapy. The term basic life support (BLS) involves all the following elements: initial assessment; airway maintenance; expired air ventilation (rescue breathing); and chest compression. When all three [airway breathing, and circulation, including chest compressions] are combined, the term cardiopulmonary resuscitation (CPR) is used.
There are many different kinds of abnormal heart rhythms, some of which can be treated by defibrillation therapy (“shockable rhythms”) and some which cannot (non-shockable rhythms”). For example, most ECG rhythms that produce significant cardiac output are considered non-shockable (examples include normal sinus rhythms, certain bradycardias, and sinus tachycardias). There are also several abnormal ECG rhythms that do not result in significant cardiac output but are still considered non-shockable, since defibrillation treatment is usually ineffective under these conditions. Examples of these non-shockable rhythms include asystole, electromechanical disassociation and other pulseless electrical activity. Although a patient cannot remain alive with these non-viable, non-shockable rhythms, applying shocks will not help convert the rhythm. The primary examples of shockable rhythms, for which the caregiver should perform defibrillation, include ventricular fibrillation, ventricular tachycardia, and ventricular flutter.
After using a defibrillator to apply one or more shocks to a patient who has a shockable ECG rhythm, the patient may nevertheless remain unconscious, in a shockable or non-shockable, perfusing or non-perfusing rhythm. If a non-perfusing rhythm is present, the caregiver may then resort to performing CPR for a period of time in order to provide continuing blood flow and oxygen to the patient's heart, brain and other vital organs. If a shockable rhythm continues to exist or develops during the delivery of CPR, further defibrillation attempts may be undertaken following this period of cardiopulmonary resuscitation. As long as the patient remains unconscious and without effective circulation, the caregiver can alternate between use of the defibrillator (for analyzing the electrical rhythm and possibly applying a shock) and performing cardiopulmonary resuscitation (CPR). In the most recent version of the guidelines promulgated by the American Heart Association (AHA) in 2005, CPR may now also be delivered prior to defibrillation shocks, even for patients presenting to the rescuer with a shockable rhythm such as ventricular fibrillation. In the most recent AHA guidelines, CPR generally involves a repeating pattern of 30 chest compressions followed by a pause during which two rescue breaths are given.
Ventilation is a key component of cardiopulmonary resuscitation during treatment of cardiac arrest. Venous blood returns to the heart from the muscles and organs depleted of oxygen (O2) and full of carbon dioxide (CO2. Blood from various parts of the body is mixed in the heart (mixed venous blood) and pumped to the lungs. In the lungs the blood vessels break up into a net of small vessels surrounding tiny lung sacs (alveoli). The net sum of vessels surrounding the alveoli provides a large surface area for the exchange of gases by diffusion along their concentration gradients. A concentration gradient exists between the partial pressure of CO2 (PCO2) in the mixed venous blood (PvCO2) and the alveolar PCO2. The CO2 diffuses into the alveoli from the mixed venous blood from the beginning of inspiration until an equilibrium is reached between the PvCO2 and the alveolar PCO2 at some time during the breath. When the subject exhales, the first gas that is exhaled comes from the trachea and major bronchi which do not allow gas exchange and therefore will have a gas composition similar to the inhaled gas. The gas at the end of this exhalation is considered to have come from the alveoli and reflects the equilibrium CO2 concentration between the capillaries and the alveoli; the PCO2 in this gas is called end-tidal PCO2 (PetCO2).
When the blood passes the alveoli and is pumped by the heart to the arteries it is known as the arterial PCO2 (PaCO2). The arterial blood has a PCO2 equal to the PCO2 at equilibrium between the capillaries and the alveoli. With each breath some CO2 is eliminated from the lung and fresh air containing little or no CO2 (CO2 concentration is assumed to be 0) is inhaled and dilutes the residual alveolar PCO2, establishing a new gradient for CO2 to diffuse out of the mixed venous blood into the alveoli. The rate of breathing, or minute ventilation (V), usually expressed in L/min, is exactly that required to eliminate the CO2 brought to the lungs and maintain an equilibrium PCO2 (and PaCO2) of approximately 40 mmHg (in normal humans). When one produces more CO2 (e.g., as a result of fever or exercise), more CO2 is produced and carried to the lungs. One then has to breathe harder (hyperventilate) to wash out the extra CO2 from the alveoli, and thus maintain the same equilibrium PaCO2. But if the CO2 production stays normal, and one hyperventilates, then the PaCO2 falls. Conversely, if CO2 production stays constant and ventilation falls, arterial PCO2 rises. Some portion of the inspired air volume goes to the air passages (trachea and major bronchi) and alveoli with little blood perfusing them, and thus doesn't contribute to removal of CO2 during exhalation. This portion is termed “dead space” gas. That portion of V that goes to well-perfused alveoli and participates in gas exchange is called the alveolar ventilation (VA) and exhaled gas that had participated in gas exchange in the alveoli is termed “alveolar gas”.
Automatic ventilators capable of delivering desired airway pressures are also known. U.S. Pat. No. 5,664,563, describes a ventilation system capable of delivering negative airway pressures. U.S. Pat. Nos. 4,676,232, 5,020,516 and 5,377,671 describe a ventilator with ventilation cycles synchronized with the cardiac cycle in order to enhance circulation. U.S. Pat. No. 4,326,507 describes a combined chest compressor and ventilator that delivers a ventilation over a number of compression cycles and then delivers another series of compression cycles during the period between ventilations.
While the current AHA recommendation is two ventilations every thirty compressions, that recommendation was promulgated in large part because it was found that the delays due to switching back and forth between compressions and ventilation by rescuers was resulting in insufficient levels of chest compressions and the resultant circulation. It is desirable, in the case of mechanical devices to integrate the functions of chest compressions and ventilations.
U.S. Pat. Nos. 6,179,793 and 6,752,771 describe an inflatable vest for assisting the heart in patients suffering from heart failure. The inflation of the vest is synchronized with on-set of the systole phase of the heart, when the left ventricular compresses to force blood out of the heart and through the aorta. The inflated vest compresses the patient's chest and increases the intrathoracic pressure. This increase in pressure assists the heart in moving blood out of the heart and through the aorta. U.S. Pat. Nos. 4,198,963 and 6,171,267 describe a device that synchronizes a chest compression cycle to the systolic phase of cardiac activity. U.S. Pat. No. 6,213,960 describes a device for automatic chest compression during resuscitation.
Synchronization of the ventilation cycle with the compression cycle is described in U.S. Pat. No. 4,397,306. The patent proposes synchronizing an automatic chest compression device with an automatic ventilator, and recommends that high pressure ventilation pulses be delivered simultaneously with the compression phase (i.e., when chest pressure is applied), and that slightly negative ventilation pulses be delivered simultaneously with the decompression phase (i.e., when no chest pressure is applied). Compression and decompression phases are of equal length (50% duty cycle). The negative ventilation pulses are said “to move greater amounts of blood into the chest during diastole”. Also, the patent recommends introducing a conventional ventilation cycle every approximately sixth compression/decompression cycle, when no compression is occurring. This is said to be valuable for sufficient alveolar gas exchange since very little air flow occurs during the positive ventilation pressure cycles that are synchronized to the compression phase. While U.S. Pat. No. 4,397,306 reports that significant improvements in pressure and flow were observed using the invention, the physiological state of a typical patient differs fairly significantly from the animal model used in those experiments.
In a typical cardiac arrest, the amount of time that a patient has been without any blood flow is commonly greater than ten to twelve minutes, unlike animal models where no flow times are always less than 8 minutes, and in most experiments is less than 5 minutes. Under these prolonged conditions of ischemia, patients' vascular tone will be significantly compromised as a result of insufficient metabolic energy substrates and nitric oxide release. This loss of tone manifests itself physically with a significant increase in the compliance of the vasculature, which, like increases in capacitance in an electronic circuit, cause an increase in the intrinsic time constants of the system. This can be tested in models such as is described in Crit. Care Med 2000 Vol. 28, No. 11 (Suppl.), or in animal models with extended durations of ischemia. As the author describes, the system of differential equations has been described in a number of publications. In this specific instance, “the human circulation is represented by seven compliant chambers, connected by resistances through which blood may flow. The compliances correspond to the thoracic aorta, abdominal aorta, superior vena cava and right heart, abdominal and lower extremity veins, carotid arteries, and jugular veins. In addition, the chest compartment contains a pump representing the pulmonary vascular and left heart compliances. This pump may be configured to function either as a heart-like cardiac pump, in which applied pressure squeezes blood from the heart itself through the aortic valve, or as a global thoracic pressure pump, in which applied pressure squeezes blood from the pulmonary vascular bed, through the left heart, and into the periphery. Values for physiologic variables describing a textbook normal “70-kg man” are used to specify compliances and resistances in the model. The distribution of vascular conductances (1/resistances) into cranial, thoracic, and caudal components reflects textbook distributions of cardiac output to various body regions.” In particular, the time constants of venous return during the decompression phase are significantly increased during prolonged periods of ischemia.